Roles of mitochondria-generated reactive oxygen species on X-ray-induced apoptosis in a human hepatocellular carcinoma cell line, HLE

Hiroko P. Indo, Osamu Inanami, Tomoko Koumura, Shigeaki Suenaga, Hsiu Chuan Yen, Shizuko Kakinuma, Ken Ichiro Matsumoto, Ikuo Nakanishi, William St Clair, Daret K. St Clair, Hirofumi Matsui, Richard Cornette, Oleg Gusev, Takashi Okuda, Yasuhito Nakagawa, Toshihiko Ozawa, Hideyuki J. Majima*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

48 Scopus citations

Abstract

HLE, a human hepatocellular carcinoma cell line was transiently transfected with normal human MnSOD and MnSOD without a mitochondrial targeting signal (MTS). Mitochondrial reactive oxygen species (ROS), lipid peroxidation and apoptosis were examined as a function of time following 18.8 Gy X-ray irradiation. Our results showed that the level of mitochondrial ROS increased and reached a maximum level 2 hours after X-ray irradiation. Authentic MnSOD, but not MnSOD lacking MTS, protected against mitochondrial ROS, lipid peroxidation and apoptosis. In addition, the levels of mitochondrial ROS were consistently found to always correlate with the levels of authentic MnSOD in mitochondria. These results suggest that only when MnSOD is located in mitochondria is it efficient in protecting against cellular injuries by X-ray irradiation and that mitochondria are the critical sites of X-ray-induced cellular oxidative injuries.

Original languageEnglish
Pages (from-to)1029-1043
Number of pages15
JournalFree Radical Research
Volume46
Issue number8
DOIs
StatePublished - 08 2012

Keywords

  • Apoptosis
  • Mitochondria
  • MnSOD
  • ROS
  • X-rays

Fingerprint

Dive into the research topics of 'Roles of mitochondria-generated reactive oxygen species on X-ray-induced apoptosis in a human hepatocellular carcinoma cell line, HLE'. Together they form a unique fingerprint.

Cite this